DESCRIPTION Individuals with Parkinson's disease (PD) present with a variety of motor symptoms including resting tremor, difficulty initiating movement/slowed movements, and rigidity. While these motor signs and symptoms are the hallmark features, individuals with PD also often demonstrate changes in communication ability, with an estimated prevalence of 89 percent of all individuals with PD being affected. These disorders of communication have been reported by individuals with PD and their caregivers to be one of the most difficult aspects of living with this disorder (Fox & Ramig, 1997). The most commonly diagnosed communicative disorder in PD is hypokinetic dysarthria which can result in changes in prosody, respiratory control, voice quality, and articulation. Of these, the disorders in prosody have been judged to be the most prominent deficit (Darley, Aronson & Brown, 1969; Plowman-Prine et al., 2009). Prosody includes the pitch, loudness, and rate with which speech utterances are produced (Kent, 1997) and is used to communicate emotional connotation (e.g. angry versus sad). Impairments in speech prosody reduce the ability to communicate emotional feelings or intentions (Pell, Cheang, & Leonard, 2006) as well as reducing the intelligibility of the spoken message (Lansford, Liss, Caviness, & Utianski, 2011). While pharmacological treatments have been shown to be effective in improving motor function, these medications have not been shown to greatly mitigate speech production disorders including prosody (Goberman, Coelho & Robb, 2005; Plowman-Prine, et al., 2009), suggesting that therapies other than dopaminergic agents are needed to address prosody deficits in PD. Despite a negative impact on quality of life and reduced independence of individuals affected by emotional prosodic disorders, no published studies are available testing therapies to improve production of emotional prosody in PD (Schrder et al., 2009). The primary goal of this CDA1 proposal is to compare a treatment protocol shown to be effective in treating emotional prosodic deficit in stroke and TBI (Leon et al., 2005; Rosenbek et al., 2006) to a standard clinical treatment for prosody deficit that does not target the emotional aspect of the disorder in individuals with PD. The experimental treatment targets increased pitch and loudness variability, and control of speech rate, the core characteristics of prosodic insufficienc in PD, but with an emphasis on the emotional component of the disorder. The primary aims of the study are to determine treatment effect size by measuring the difference of the experimental protocol versus standard clinical care on prosodic deficit in individuals with PD via changes in acoustic and perceptual measures, as well as provide psychometric validation of test-retest reliability of the outcome measures.